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Review
. 2022 Jul 28:13:937684.
doi: 10.3389/fimmu.2022.937684. eCollection 2022.

Immune escape mechanisms of severe fever with thrombocytopenia syndrome virus

Affiliations
Review

Immune escape mechanisms of severe fever with thrombocytopenia syndrome virus

Tong Wang et al. Front Immunol. .

Abstract

Severe fever with thrombocytopenia syndrome (SFTS), which is caused by SFTS virus (SFTSV), poses a serious threat to global public health, with high fatalities and an increasing prevalence. As effective therapies and prevention strategies are limited, there is an urgent need to elucidate the pathogenesis of SFTS. SFTSV has evolved several mechanisms to escape from host immunity. In this review, we summarize the mechanisms through which SFTSV escapes host immune responses, including the inhibition of innate immunity and evasion of adaptive immunity. Understanding the pathogenesis of SFTS will aid in the development of new strategies for the treatment of this disease.

Keywords: SFTS; SFTSV; adaptive immune response; immune escape; innate immune response.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Effects of SFTSV infection on immune cells. SFTSV infection impairs the production and function of various immune cells, such as monocytes, macrophages, and DCs. It also promotes B-cell proliferation and differentiation into PBs/plasma cells, which are deemed potential virus reservoirs.
Figure 2
Figure 2
Immune escape mechanism of SFTSV in monocytes. The SFTSV NSs protein hijacks various protein molecules of the IFN pathway by forming IBs, thereby hindering IFN production. In addition, SFTSV activates the NF-κB pathway and promotes macrophage differentiation into the M2 phenotype to facilitate viral replication.

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